Vulvodynia is a chronic pain disorder, consisting of vulvar pain (burning, stabbing, irritation) for three months or longer, and lack of an infectious or dermatologic diagnosis consistent with the pain. The clinical characteristics of vulvodynia, and response to pharmacological therapy, are consistent with those of neuropathic pain. However, previous data from our group indicate increased sensitivity to pressure not only at the vulva, but also in the periphery (thumb, deltoid, and shin), suggesting that central mechanisms may be playing a role in women with vulvodynia. Further clarification of central and peripheral pain processing in women with and without vulvodynia has the potential to dramatically increase our understanding of this disorder, and will direct further study of pathophysiologic mechanisms and treatment options in vulvodynia. The specific aims of this study are: 1) to assess multi-modal sensory profiles at the vulva and in the periphery of 100 women with vulvodynia and 50 women without vulvar pain, and to use principal component and cluster analyses to identify novel subgroupings within the groups of cases, identify potential confounders, such as age, that can significantly affect the variation in the sensitivity data, possibly differentially in women with and without vulvodynia, and, 2) to further identify underlying mechanisms of vulvar pain in the established subgroupings by identifying, via fMRI, the qualitative and quantitative differences in location and character of supraspinal activity evoked by non-painful and painful sensory provocation at both vulvar and peripheral sites. We expect to find significant differences among the validated groups, and to then be able to use the known functional role of specific activated neural structures in the central nervous system to further refine hypotheses about the mechanisms that initiate and maintain painful vulvar disorders. Information from this research is anticipated to further define vulvodynia and its variants, to define subgroups based on underlying mechanisms, and to further our understanding of the pathophysiology of women with this disorder.